Room 613 Walton Research Building
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Phone:
843-792-2704
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Fax: 843-792-0368 |
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Education:
Research Interests: Our laboratory conducts basic biomedical research aimed at defining the molecular and cellular mechanisms responsible for generating the unique ionic and electrochemical gradients in the inner ear. Biochemical and histochemical techniques are used to identify and determine the precise cellular distribution of ion transport mediators and their associated regulatory proteins. Emphasis is placed on relating changes in auditory function with alterations in the expression of key proteins promoted by disease, noise-trauma and aging. In vivo and in vitro studies are conducted using mouse and gerbil animal models. Recent work focuses on direct correlational studies of human auditory performance with structural and molecular changes in the human inner ear.
Funding: Work in the laboratory is supported in part by grants R01 DC00713 and P50 DC00422 from the National Institute on Deafness and Other Communication Disorders.
Recent Publications
Weber PC, Cunningham CD, Schulte BA. Potassium recycling pathways in the human inner ear. Laryngoscope 111:1156-65,2001. (abstract)
Schmiedt RA, Lang H, Okamura H, Schulte BA. Effects of furosemide chronically applied to the round window: A model of metabolic presbyacusis. J Neuroscience, 22(21):9643-9650, 2002 (abstract)
Heaney D, Schulte BA, Niedzielski A. Dystroglycan expression in the developing and senescent gerbil cochlea. Hearing Res, 174:9-18, 2002. (abstract)
Lang H, Schulte BA, Schmiedt RA. Effects of chronic furosemide treatment and age on cell division in the adult gerbil inner ear. JARO, 4:164-175. 2003. (abstract)
Heaney D, Schulte BA. Dystroglycan expression in the mouse cochlea. Hearing cochlea. Hearing Res, 177:12-20, 2003. (abstract)
Shen Z, Liang F, Hazen-Martin D, Schulte BA. BK channels mediate the voltage-dependent outward current in type I spiral ligament fibrocytes. Hearing Res, 187:35-43, 2004. (abstract)
Lang H, Schulte BA, Schmiedt RA. Ouabain induces apoptotic cell death in type I spiral ganglion neurons, but not type II neurons. JARO 6:63-74, 2005. (abstract)
Spicer SS, Schulte BA. Pathologic changes of presbyacusis begin in secondary processes and spread to primary processes of strial marginal cells. Hearing Res, 205:225-240, 2005. (abstract)
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